DECAY OF THE TEETH

ental decay, or dental caries as it is more properly called, is a disease which, as su r^?ne ̂ ows, produces holes or cavities in the teeth. These occur where the tooth ch ^CeS are Protected from the normal cleansing action of the tongue, the lips and the s 0r where the softer tissues of the root (Plate XXII) are exposed by recession of the increasing age. There are three main sites: in the natural folds found in

ch ^CeS are Protected from the normal cleansing action of the tongue, the lips and the s 0r where the softer tissues of the root (Plate XXII) are exposed by recession of the increasing age. There are three main sites: in the natural folds found in an(j surfaces of the posterior teeth, at the points of contact between the teeth, 0 1at junctions between the teeth and the gums. For convenience these are called Sal> mterproximal, and cervical danger areas (  very difficult to find the early lesions and they cannot be recognized clinically until cavities begin to form. Fortunately radiographs help us to find some of these lesions at a fairly early stage, but we are now beginning to understand that any lesion which can be found by probe or radiography has already done much damage (Plate XXIII(^))-Symptoms and Complications At the same time as this process is occurring the patient begins to notice certain symptoms. About the time that the early cavity begins to form, the tooth may becofltf sensitive to sweet foods and possibly also to salty foods. Such pain is at first transient' disappearing with the removal of the stimulus, but as the cavity increases in size and the disease penetrates further into the tooth the soft tissue in the centre of the tooth which we call the pulp or nerve, becomes inflamed. This is slight at first but it result5 in an increased sensitivity of the tooth to sweet foods and painful sensation from or cold. As the condition progresses the pain becomes more intense and lasts longef until eventually the inflammation of the pulp becomes so severe that the pain is coj1' tinuous. It mounts in intensity because of the increasing pressure within the pu'P until the patient is at last driven to seek relief in one way or another. Fortunately' this final stage of acute pulpitis rarely lasts more than half to one hour, as the pressU^ within the pulp causes an obstruction of the blood flow and the pulp tissue dies. TP' is usually noticed as a sudden cessation of pain and often occurs as the patient rin$ the dentist's door bell.
,, At this stage of acute pulpitis the tooth is usually past saving for almost inevitaf' the inflammation will have passed beyond the tooth into the supporting structut, (Fig. 2). Once this has happened, sooner or later it leads to the formation of a den abscess around the apex of the root. This in turn may cause considerable pain ^ over several months if it becomes chronic. Finally it discharges and the pain The infection however persists and a discharging sinus usually remains conn^e ^ root of the carious tooth to the surface of the gum or face. In this stage t suffers no real pain except in acute exacerbations of the abscess.  The whole process from the onset of caries may take several years or may occur much more rapidly. Throughout this time the patient suffers periodic attacks of pain ?ften being subject to some pain almost continuously. As for the infection, it is certain that this can at times cause systematic disease, but it seems unlikely that it causes much more than malaise and misery in most patients.
Fortunately today many of the sequelae of dental caries are prevented by good dental treatment at an early stage of the disease, but there are still far too many patients Who prefer to avoid conservative treatment and wait till their teeth "fall out" or require extraction.
Having examined the natural history and complications of the disease we must now consider its scope.
incidence For many years now the percentage of school children in this country who are inically free from caries has been 5 per cent or less. Being based only on clinical is ^lnat^0n this simply means that they have no recognizable cavities and the figure tyh ?re^0re probably too high. It is also known that in adults there are even fewer \st0ncally the advance of caries can be closely related to civilization. It is very rare incid animals an^ in primitive man, but with the advent of each civilization its prob>ei!\Ce.seems to have increased. It was certainly known to the Egyptians, though of SQa y.Jt was not very widespread. By the time of the Romans it was already a matter ^liddl16 !mP0rtance and dental restorations were being used. In Britain during the the n G ?es it was quite commonplace. Since then it has steadily advanced until present day. each vay We accePt the fact that the schoolchild usually has at least one cavity for and thfar ^e" avera8e each schoolchild produces one or two cavities each year tooth T?ay ^egin as early as 2 to 3 years of age or within one year of cutting the first ably too h?Wever's extreme, but it must not be forgotten that this picture is probaccessibl ?Ptlrn'stic for we can only count cavities. The early lesions are often inheen ne ^ an<^ ^crefore unrecognized. There are several cases on record where it has of caries^Tnf1^ t0 extract a^ teeth for children of three to four years, solely because story 0f 1 .? teeth themselves showed no gross faults of structure. In fact the common *t is oft teeth is usually only an unsatisfactory excuse.
'ncidence ^ Su^ested that pregnancy and other systemic conditions may increase the a^ected b? Car*es". There is no doubt that the structure of developing teeth may be begin to occur in the exposed roots. This cervical caries of middle age is relatively i minor problem. The major problem is the loss of teeth in childhood, for it is now knowfl that the premature loss of baby teeth and of permanent teeth in early life can caus? many dental deformities and can contribute to the causation of pyorrhoea in later lifr It has now become a matter of national importance that caries should be prevented' Whether we consider it as a financial matter of the cost of treatment under the health service or as the loss of man hours from toothache and treatment, or simply as a queS' tion of pain and misery, it still affects everyone and causes altogether too mud1 trouble.
If it is to be prevented then we must know something of its causes and pathology' Pathology The first real attempt to understand the process was made by Miller in 1890' He suspected that caries was caused by the fermentation of food stagnating around tH teeth. To demonstrate this he took pieces of teeth and incubated them in a mixture0 bread and saliva and eventually produced the first artificial caries, with lesions in maw ways similar to the natural variety. On these experiments he built the theory that caf)e , is caused by acid which is produced by the action of bacteria on refined carbohydratf stagnating round the teeth. This theory is still acceptable today with a few modi*1 cations.
Interest has always centred on the attack of caries upon the enamel for this is ( tissue which must first be breached before the tooth is endangered. Unfortunately)' Miller's day it was thought that enamel consisted wholly of calcium salts, but ab? ^ 1906 Bodecker demonstrated that it also contained a small amount of organic or Pr? tein material.
It had been recognized for some time that Miller's theory did not explain all^' facts and when it was discovered that the protein or organic matrix showed dist11^, changes in caries a new theory was advanced. Caries was now said to be caused bacterial attack upon the protein. .p.
Further experimentation has now shown quite clearly that two processes are volved. These are the removal of calcium salts and the alteration and destruction 01 J organic matrix. It is also clear that caries cannot occur without the stagnation refined carbohydrates and without the presence of bacteria. It is highly probable { acid is produced which removes the calcium salts, but other methods are at PreS > being suggested.

Prevention j{
On this basis several methods of prevention have been tried. In animals suscep^j, to caries it has been shown conclusively that if bacteria can be excluded from the rt1 ^ no caries occurs, but in man it has been shown equally conclusively that while 3 f[ septics and antibiotics will eliminate the organisms almost completely for a ? ^ time after their application the organisms return within the hour as the drug? p washed away by the saliva. The same is true of various chemicals which have used to neutralize the acid and in addition there is considerable difficulty in Se the neutralizing agent to the sites where the acid is produced.
f|f It is also known that where patients have been willing to exclude refined c'* j jt hydrates completely from their diets the caries incidence falls very rapidly seems quite clear from the evidence that most of the general variations in c^o' incidence with race or civilization can be explained by the amount of refined c3 hydrate in the diet. ^ Many dental surgeons have limited the intake of refined carbohydrate children with a startling lack of caries as the result. Unfortunately even these c ' A grow out of parental control and may become confirmed suckers of sweets meals. Then unfortunately the caries begins. This is the real problem. How can PLATE XXII Ground section of tooth showing the body of the tooth consisting of dentine. The crown is covered by a layer of enamel which shows diagonal incremental lines. The pulp cavity is cut rather obliquely and should continue right through the apex of the root.
Ground section of toolli showing the body of the tooth consisting of dentine. The crown is covered by a layer of enamel which shows diagonal incremental lines. The pulp cavity is cut rather obliquely caries be prevented without a serious change in our habits, for it would seem that the Public do not yet regard dental disease as of sufficient importance to justify a change of nabits.
Much can be done by the individual to reduce the stagnation of food around the e. by tooth brushing and mouth rinsing. The latter is very valuable and consists of 4uuting water back and forward between the teeth immediately after meals. No-one uid claim that this does more than reduce the incidence of caries and even so children t^le rea^ Pr?blem as it is difficult to get their co-operation in these exercises ?ut the immediate supervision of an adult or until they become susceptible to Son> which is often after much damage has been done. ^foorides B(?oerhaPs the most important of all preventive measures has been the use of fluorides.
inc:/e theWar it was noted that where the population had mottled teeth the caries It w eniCe *n children was only half that of similar communities without mottling, rides ' er ^covered that the mottling was caused by a high concentration of fluores m the water supply. Further investigation showed that the fluorides were also ?btai Sj . ^or tbe reduction in caries incidence and that the same effect could be Water C ^^out mottling by using one part per million of fluoride in the drinking drinkj1^ COmmunities in America have been adding this amount of fluorides to their ^cide^ Water ^or periods of 10 years and more and they have consistently reduced the has bp106 car!es *n their children by about 50 per cent. Recently a similar procedure howeve^ ** centres in this country but it is too early to expect results. It is *^ere has ^n^dentiy expected that similar results will be obtained. Unfortunately and even f 6n a ?reat acrimonious and uninformed discussion of the dangers ^is pap ethics of this procedure, but we are not concerned with these aspects enam^reSt ^es *n two ^aQts. We are told that fluorine renders the calcium salts of discover "^ch less soluble but only produces a 50 per cent reduction. We are also V'"~"~nf~the mottied'teith of gross fluorosis, -uvering that one of the principal feat"^ calcified.
<mscep-Wh show little caries, is that they are baf^ ieeth should be more suscep-If our previous theories are correct poor > 4 badly calcified teeth to be u ^ to caries and not less. Nor are these the only badly ree from no-:--' V* uom caries. We have recently had the opportunity which is often k es,)yith a rare disease of the enamel called amelogenesi edeified and yet the J^tary and unrelated to fluorine. These teeth are also badly calcified y t ence of caries in these patients was also remar a y o\ ? j^es reduce the It w?uid seem that we kno^ Httle of the mechamsm by which fluoncltt 1 ence of caries and indeed we know little of the process o r?gress in Research ear ances0<;0fte!J m dentistry the process of disease has been jessed^ich will positively identifCe u wn a rnicroscope, instead of finding new tec \ ignored so that a conv ^ tKe Pr0cess" To? frequently sound observations have been ignored en lent theory could be sustained. T ? 11 known to all dentist u ?n caries began from two facts and two problem . ^ ^ tw0 sUrfao S * car*es develops at the contact points between ee ^ times the surf?ceSw'hichbaCt ?ne may b<iCOn|C Cari?US Wd to the cariogenic agents for less time than tU becomes carious has been exposed to the car g b , carious as th^ non-earious surface. If the theories are correct both should become ca, ^ the str ^ su^ject to the same environment. The fact that they i Ucture of the tooth may be of importance.
The theory that acid formed from the fermentation of carbohydrates attacks the tooth, suggests that there should be a gradual erosion of the enamel, but as long ag? as 1932 it was shown that when sections of early carious lesions were ground and X' rayed to see where the decalcification had occurred, a thin surface zone of enarne1 remained almost unaltered while the enamel beneath was decalcified (Plate XXI V(#))' This again implied a modification of the process by the structure of the enamel.
It had also been known for many years that two processes were involved in carie5.
The removal of calcium salts and the breakdown of the organic matrix. But while each school of thought had its own idea of which happened first, no-one seemed t0 know.
. The appearances of the early carious lesions when seen down a microscope in groufl^ sections of teeth, showed two zones surrounding the main lesion (Plate XXI V(&))-^ dark zone next to the lesion which no-one could explain, and a translucent zone outsit it which had often been described as a laying down of additional calcium salts by tooth to resist the progress of the disease. The investigations cannot be described at length in this paper, but some of results are of interest. ^ Since the beginning of dental histology, the usual medium for mounting groUn sections of teeth has been Canada Balsam. The section which is ground in water be washed in alcohol and Xylol before mounting in the balsam. It was found that W using a watery medium not requiring the washing in alcohol the dark zone and ^ translucent zones disappeared. Further investigations with polarized light showed these zones were caused by small spaces some of which became filled with balsam { become translucent and some probably with bubbles of gas to make them rey? differently from the normal enamel giving the dark opaque appearance. This fin1d' was at first accidental, but it is surprising that it had never been reported before( watery media have been used in biology for many years. The next step was to try to establish the nature of the early carious lesion an*1 decide whether the removal of the calcium salts occurred before the recognizable ^ ges in the protein of the organic content or whether, as some thought, the reverse trUC' ... .

-ns'11
To do this we examined the evidence and discovered that most of the lesion ^ which organic change had been demonstrated were quite advanced and cavities ^ present. It was also apparent that some other changes were present which were ^ advance of the changes in the organic material. It seemed highly probable that earlier changes were caused by the removal of calcium salts. ^jf.
Some very early lesions were then taken and split through the centre. From one ground sections were prepared and microradiographed for evidence of decalcified ^ The other halves were prepared and stained to show changes in the organic paft enamel. In this way it was shown that calcium salts had been removed froin tj< lesions before any change in the organic or protein part could be seen. Further in ^ gation on these lines is still going on and we now know that decalcification 0 m, very early in caries. It is then followed by organic change at about the time ^ surface begins to break down and soon after this the bacteria start to enter the ^ structure. Until this stage the bacteria have been producing their effects from a ^lS -0u5 The greatest problems still remained. We could not yet explain how the c a process passed through the enamel surface zone without apparently affecting a j was able to cause a considerable loss of calcium salts within the deeper enaI? ccP' had confirmed the previous evidence of a resistant surface layer and came to \ ' ? 0 ft elusion that the process must enter through minute faults or openings whi?^ had not been demonstrated. It was obvious that the next step was to find theS? )1 ^ ings. We formed the opinion that though the openings must be extremely s ^ first they would probably increase as the lesion progressed. As a result we beg3^ gft^ ing at the more advanced lesions just before cavities would be expected. As is s case they were found when we had almost given up hope. They showed on fine ?rays of the ground sections as small openings related to the developmental pattern 0 the enamel and consisted of several small openings rather than the single point of of'^WC ^ad env^sa?ec^ (Plate XXV(a]). At this stage we estimated that about 5 per cent the calcium salts had been removed in these openings, while 25 per cent to 50 per a^nt had been removed in the underlying lesion. We were anxious to demonstrate them a an earlier stage and eventually, with the aid of biologists and physicists, devised atrri^ans for demonstrating the spaces from which material had been removed; first vv't&K ^ Per cent an<^ later as low as 1 per cent of spaces. (Plate XXV (6)). The lesions n one per cent of spaces could not be found in even the most careful macroscopic les^mina^0n' SO t0 be sought in apparently sound teeth. Eventually such th 10H S Were f?und and they showed the points of entry in precisely the same parts of ^te . pVel?Pment:al pattern as they occupied in the later lesions seen by fine X-rays, bee 1S e y stage we could only recognise the spaces. We could not be sure what had cess? rernoved from them. It was therefore necessary to add an earlier stage to the protion ?fCa^es" This stage occurs before recognizable decalcification, and is theproducminute spaces of unknown cause. X-r 611 We ^ad our ?reatest good fortune. With more experience of the use of fine ^ere better techniques we began to get better pictures and quite suddenly we fitted3 t0 distinSuish structure within the carious lesion by this means. The results the closely with our findings in polarized light, and we could now see not only And nc:e a l?ss ?f calcium salts but also the spaces from which they were lost.
First spaces are produced, probably by the removal of soluble protein. This uncovers some of the crystallites of calcium salts and allows them to be dissolved. After this the keratin is attacked and begins to show recognizable histological changes-This process probably also results in the solution of the crystallites from within the keratin. Thus it seems that the initial attack may be not a decalcification but a solution of soluble protein.
Such a theory can explain several of our previous difficulties. It places the structure of the enamel of the individual tooth as a very important factor in deciding whether caries shall occur there or not. It also explains how the surface zone of the enamel can remain largely resistant to attack because its organic matrix is largely keratin and insoluble.
It could also explain the apparent anomaly that badly calcified teeth develop litt'e caries because the important factor in starting the lesion is not the calcium salts b^j the nature of the protein, and already it can be shown that the protein of the ename in these teeth shows differences from the normal. The next question is what causes the attack? There seems no good reason to chang^ our ideas and we still think in terms of a dilute acid produced by the breakdown 0 refined sugars and carbohydrates by bacteria.
Finally comes the question of treatment and prevention, in the light of our finding5; If our theory is true it may be possible to fill the spaces in the early lesions when the" are accessible with some inert material, allowing it to be drawn in by capillary attraCs tion after drying. This might be possible and would probably prevent further progre of the lesions. 5 But more important still, if the theory is correct we must stop looking for some mea of making the calcium salts insoluble. What we require is a means of making the solu protein insoluble. If this can be done we may well be able to prevent dental Finally, the real answer would be to learn more of these points of entry whichse to be developmental faults, so that their occurrence might be prevented in devel r ment. j Of course so much of this is conjecture that it may all be wrong, but at least we more of the pathology of caries than we did, and there is some encouragement* ^ within recent months we have been able to produce artificial lesions, in extracted tee^, which are almost identical with natural decay by using a solvent which attacks the soluble protein.